Possible roles of actin and myosin during anaphase chromosome movements in locust spermatocytes

Abstract

We tested whether the mechanisms of chromosome movement during anaphase in locust (Locusta migratoria L.) spermatocytes might be similar to those described for crane-fly spermatocytes. Actin and myosin have been implicated in anaphase chromosome movements in crane-fly spermatocytes, as indicated by the effects of inhibitors and by the localisations of actin and myosin in spindles. In this study, we tested whether locust spermatocyte spindles also utilise actin and myosin, and whether actin is involved in microtubule flux. Living locust spermatocytes were treated with inhibitors of actin (latrunculin B and cytochalasin D), myosin (BDM), or myosin phosphorylation (Y-27632 and ML-7). We added drugs (individually) during anaphase. Actin inhibitors alter anaphase: chromosomes either completely stop moving, slow, or sometimes accelerate. The myosin inhibitor, BDM, also alters anaphase: in most cases, the chromosomes drastically slow or stop. ML-7, an inhibitor of MLCK, causes chromosomes to stop, slow, or sometimes accelerate, similar to actin inhibitors. Y-27632, an inhibitor of Rho-kinase, drastically slows or stops anaphase chromosome movements. The effects of the drugs on anaphase movement are reversible: most of the half-bivalents resumed movement at normal speed after these drugs were washed out. Actin and myosin were present in the spindles in locations consistent with their possible involvement in force production. Microtubule flux along kinetochore fibres is an actin-dependent process, since LatB completely removes or drastically reduces the gap in microtubule acetylation at the kinetochore. These results suggest that actin and myosin are involved in anaphase chromosome movements in locust spermatocytes.

Troponin I and Tropomyosin regulate chromosomal stability and cell polarity

“…By analogy to the role that TnI plays in the sarcomere, where the TnTm complex interacts with the actin filaments, it seems likely that during transcription actin has a filament structure, as in the sarcomere thin filament. Actin is also important for morphogenesis of cells and organs in the early embryo, ranging from nuclear divisions (Gerisch et al, 2004) and chromosomal segregation in conjunction with myosin (Fabian and Forer, 2007), to the regulation of cell shape and movements. All these processes are also relevant to the formation and progression of tumors (Bissell and Radisky, 2001;Brumby and Richardson, 2005).…”

Gamma-actin is involved in regulating centrosome function and mitotic progression in cancer cells

“…[2][3][4] The actin filaments together with several actin regulatory proteins such as myosin-10, 5,6 myosin II, 7-11 moesin 12-14 and formin 2 [15][16][17] have been implicated to be critically important in regulating mitosis and/or meiosis in various systems. The role of actin and its regulatory proteins in these processes ranges from regulating centrosome separation 18,19 to proper spindle assembly and orientation [6][7][8]12,13,[15][16][17] to elongation of kinetochore microtubules. 11,20 Importantly, disruption of the actin cytoskeleton affects mitotic and/or meiotic spindle structure and function, resulting in mitotic defects [6][7][8][11][12][13]20 and/or meiotic defects.…”

“…The role of actin and its regulatory proteins in these processes ranges from regulating centrosome separation 18,19 to proper spindle assembly and orientation [6][7][8]12,13,[15][16][17] to elongation of kinetochore microtubules. 11,20 Importantly, disruption of the actin cytoskeleton affects mitotic and/or meiotic spindle structure and function, resulting in mitotic defects [6][7][8][11][12][13]20 and/or meiotic defects. [15][16][17] These studies provide evidence of how critically important actin and its regulatory proteins are in regulating cell division.…”

The molecular basis of anaphase A in animal cells

“…Numerous additional components required for efficient anaphase A are likely to emerge, and those identified in certain cell types may play no role in others. There is also evidence that chromatidto-pole motility is not solely the result of the depolymerization of kinetochore-associated microtubule ends (Fabian and Forer 2005;Fabian and Forer 2007). Finally, some cell types display very little anaphase A, and in these anaphase, chromosome segregation is driven almost entirely by anaphase B (Straight et al 1997).…”